Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a case report of a 34 years old man with Evans syndrome associated with antiphospholipid-protein antibodies. They include lupus anticoagulant and antibodies against cardiolipin, prothrombin and beta 2-glycoprotein I, detected by ELISA. No thrombotic events were observed. The presence of several antibodies directed against surface cell membrane structures in Evans syndrome suggests a common pathogenetic mechanism.
Pol Merkur Lekarski 1996 Nov
PMID:[Evan's syndrome with antiphospholipid-protein antibodies]. 927 14

Classification criteria for antiphospholipid syndrome were first proposed in 1987, revised in 1999 (Sapporo criteria) and up-dated in 2006. The aim of the study was to analyze associations between clinical and laboratory symptoms of antiphospholipid syndrome in the group of patients with autoimmune diseases, based on recently up-dated classification criteria. 336 patients were enrolled into the study, with the majority (n=235) suffering from SLE. Laboratory determinations included: lupus anticoagulant (LA), anticardiolipin (aCL) and anti-beta2-glycoprotein I (abeta2GPI) (both of IgG and IgM class). Clinical and laboratory symptoms of antiphospholipid syndrome were quite common among patients studied. There was a significant association between laboratory and clinical features of antiphospholipid syndrome, according to recently modified classification criteria.
Pol Arch Med Wewn 2006 May
PMID:[Antiphospholipid syndrome in autoimmune diseases]. 1719 56

Although atherosclerosis was previously thought to be mainly a degenerative disease, it is now well ascertained that its pathogenesis is inflammatory. This review describes the history of a new atherogenetic concept, including the pivotal role of apoE-knockout mice in understanding the inflammatory background of atherosclerosis. There has been lack of unequivocal evidence of an important inflammatory component in atherogenesis. This evidence was delivered by a new technique--gene targeting, for the invention of which Mario R. Capecchi, Martin J. Evans and Oliver Smithies received in 2007 the Nobel Prize in Physiology or Medicine. The pivotal stage of atherogenesis is the antigen presentation by macrophages to T lymphocytes. This antigen could be a fragment of oxidized low-density lipoproteins "digested" by macrophage, heat shock protein 60, beta2-glycoprotein I or fragments of bacterial antigens. For interaction between the immunological cells a presence of CD40 receptor on macrophages and its ligand CD40L on the surface of T lymphocytes are necessary. During the interaction between these cells an immunological type T helper 1 (Th1--cellular) or T helper 2 (Th2--humoral) response arises. Th1 response and its mediators: interferon gamma, tumor necrosis factor alpha, interleukin-1, interleukin-12 and interleukin-18 enhance atherogenesis, whereas Th2 response and its mediators: interleukin-4, interleukin-5, interleukin-10 and interleukin-13 inhibit the development of atherosclerosis. Atherosclerosis is therefore a chronic inflammatory disease, in most cases initiated by hypercholesterolemia. Nowadays, hypercholesterolemia and inflammation are considered as "partners in crime". The concept of atherosclerosis as inflammatory disease is fairly new, however, it is already considered as an undisputable achievement of science which have particular therapeutic consequences.
Pol Arch Med Wewn 2008 Mar
PMID:New insights into immunological aspects of atherosclerosis. 1847 59

The aim of the present study was to perform comparative analysis of serum from patients with different stages of non-small cell lung cancer (NSCLC) using the three complementary proteomic approaches to identify proteome components associated with the progression of cancer. Serum samples were collected before any treatment from 200 patients with NSCLC, including 103 early stage, 64 locally advanced and 33 metastatic cancer samples, and from 200 donors without malignancy. The low-molecular-weight fraction of serum proteome was MALDI-profiled in all samples. Serum proteins were characterized using 2D-PAGE and LC-MS/MS approaches in a representative group of 30 donors. Several significant differences were detected between serum samples collected from patients with early stage cancer and patients with locally advanced cancer, as well as between patients with metastatic cancer and patients with local disease. Of note, serum components discriminating samples from early stage cancer and healthy persons were also detected. In general, about 70 differentiating serum proteins were identified, including inflammatory and acute phase proteins already reported to be associated with the progression of lung cancer (serum amyloid A or haptoglobin). Several differentiating proteins, including apolipoprotein H or apolipoprotein A1, were not previously associated with NSCLC. No significant differences in patterns of serum proteome components were detected between patients with adenocarcinoma and squamous cell carcinoma. In conclusion, we identified the biomarker candidates with potential importance for molecular proteomic staging of NSCLC. Additionally, several serum proteome components revealed their potential applicability in early detection of the lung cancer.
Acta Biochim Pol 2014
PMID:Identification of serum proteome components associated with progression of non-small cell lung cancer. 2487 61